Lecture 21 : Control of the Heart Flashcards

1
Q

What are intrinsic or local controls?

A

Controls that originate entirely from within a system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are extrinsic controls?

A

Controls that involve input from outside - in particular hormonal and nervous effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do intrinsic and extrinsic controls work together?

A

Both forms of control operate continuously to adjust the heart and vessels, so that both are always functioning appropriately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a chronotropic factor?

A

Anything affecting heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an inotropic factor?

A

Anything affecting stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is stroke volume?

A

The difference between the end diastolic volume (EDV) and the end systolic volume (ESV)
* SV= EDV-ESV
* With every beat the heart pumps about 60% of the blood in its chambers (65-70 mL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 3 intrinsic and extrinsic controls of stroke volume?

A
  1. Preload
  2. Afterload
  3. Contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is preload an intrinsic control?

A
  • Determines the intial (pre-contraction) muscle fibre length
  • Left ventricle - when EDV and EDP increase = preload increase
  • LVEDV and LVEDP will be used as the index of preload of the left ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is pre load related to ‘Starling’s law of the heart’ or ‘Frank-Starling mechanism’?

A

If LVEDV increases, the left ventricle responds by doing more work
- Extra work done by the left ventricle produces a larger stroke volume
- More fill = more empty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What accounts for the Frank-Starling mechanism?

A
  • Length-tension relationship
  • Increase in Ca2+ sensitivity
  • Increase in number and strength of cross-bridges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is afterload?

A
  • Intrinsic control
  • The tension the fibres must generate before they can shorten
  • Afterload is the pressure that the ventricles must overcome to force open the aortic and pulmonary valves
  • Increase in arterial pressure = increase afterload (hypertension)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is afterload determined?

A

Mean aortic or mean arterial pressure will be used as the index of afterload of the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the extrinsic control of contractility:

A
  • Catecholamines from the adrenal medulla, and sympathetic nerves in the heart, alter ventricular function without a change in LVEDV
  • Improve contractiliy
  • More “effective” pump
  • Causes contraction and relaxation to occur more quickly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If contractility increases what is the affect on stroke volume?

A

Stroke volume increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the ejection fraction?

A

Blood pumped out of the heart per beat
- The ratio of stroke volume (SV) to end-diastolic volume (EDV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the ejection fraction (EF) equation?

A

EF = SV/EDV
EF = 70/130
* Expressed as %, EF normally averages between 50-75% under resting conditions

16
Q

Describe the overall inotropic effect:

A
  • Increase sympathetic nerve activity to heart
  • Increase EDV
  • Increase plasma epinephrine
    -> Increase stroke volume
16
Q

If contractility increases what happens to EF?

A

Ejection fraction increases

17
Q

Which mechanism has the major control on heart rate?

A

Extrinsic mechanisms (nervous and endocrine)

18
Q

What role do intrinsic mechanisms play in controlling heart rate?

A
  • Very limited role
  • Right atrial pressure has small effect of AP generation by SA node
19
Q

How do extrnisic mechanisms of heart rate operate?

A
  • Tonic
  • Mostly active and control CV system by altering level of their control, rather than switching on/off
  • Without nervous control HR would be ~110bpm at rest
20
Q

What is a result of increasing parasympathetic nervous activity to the SA node?

A

Reduces HR: 110bpm-70bpm

21
Q

What is the result of increasing sympathetic nervous activity?

A
  • Increases frequency of AP generation in the SA node
    -> Increase HR: 110bpm-170bpm
22
Q

What effect do agents that alter heart rate have?

A

They have a chronotropic effect

23
Q

How are chronotropic effect of the nervous system brought about?

A

Alterations to the slope of the slow diastolic pacemaker potential through changes in the permeability of the SA node cell membrane to K+, Na+ and Ca2+

24
Q

What are 6 responses of the heart to increased sympathetic activity?

A
  1. Increase heart rate
  2. Increase conduction velocity
  3. Reduction in duration of diastole
  4. Small reduction in duration of systole
  5. Synchronisation of contractions
  6. Elevated contractility - SV maintained despite HR increase
25
Q

What is cardiac work?

A

The work the heart has to do
- Metabolic cost (O2 demand) is determined by tension development in the cardiac muscle (Law of laplace)

26
Q

What is the law of laplace?

A
  • Muscle tension (T) to develop ventricular pressure (P) depends on radius of the ventricle (r) and the thickness of the ventricle wall (u)
  • Tension = transmural pressure x radius
    2 x wall thickness
  • 𝑻 =𝑷 𝑿 𝒓/ 𝟐 𝑿 u
27
Q

What is the relationship between tension and pressure, radius and thickness?

A

T α P
T α r
T α 1/u

28
Q

What affects metaboloic cost more, tension development or muscle shortening?

A

Tension development

29
Q

What is needed in order for a constant afterload?

A

Tension that has to be generated by the ventricular muscle increases as the radius (LVEDV) increases

30
Q

What is needed for a constant radius?

A

Tension that has to be generated by the ventricular muscle increases as the afterload increases

31
Q

What is acute heart failure (preload)?

A
  • Left ventricle unable to contract effectively at a normal LVEDV
  • It fills more - larger LVEDV - in order to generate a normal stroke volume
  • Continuously larger volume (radius)
  • Ventricle generates more tension
  • Dilated ventricle has thinner wall (u)
    = problem
32
Q

What is arterial hypertension (afterload)?

A
  • Ventricle has to generate higher pressure than normal
  • Requires greater tension development
  • Hypertrophy of the ventricular wall increases wall thickness, bringing wall tension development back towards normal
  • Larger mass of heart muscle will require more oxygen (and coronary blood flow reduced due to thick muscle)